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<p>Diabetes mellitus is a chronic disorder marked by elevated blood sugar due to insufficient insulin production, reduced insulin sensitivity, or both. The global incidence of diabetes has four-fold the past 20 years, creating a significant health crisis. According to the International Diabetes Federation (2025), around 589&#xa0;million adults aged 20 to 79 were living with diabetes in 2024. Among this group, more than 9.5&#xa0;million were affected by type 1 diabetes, including approximately 1.9&#xa0;million children and adolescents below 20 years of age. By 2050, the global number of individuals with diabetes is anticipated to increase to nearly 853&#xa0;million. It is classified into type 1 (DM1), which destroys pancreatic β-cells, and type 2 (DM2), primarily linked to insulin resistance. Persistent hyperglycemia in DM causes organ damage, leading to both microvascular and macrovascular complications. OS is crucial in DM’s onset and progression. ROS produced during oxygen metabolism, disrupt cellular metabolic processes and cause oxidative damage. This imbalance between ROS production and antioxidant defences worsens DM complications by impairing insulin production and action. In DM1, ROS reduce β-cell functionality, and hyperglycemia further induces oxidative stress. Key molecular pathways involved in oxidative stress during DM are glycolysis, the hexosamine pathway, PKC activation, and the polyol pathway. Hyperglycemia-induced mitochondrial superoxide inhibits GAPDH, causing glyceraldehyde-3-phosphate to accumulate and activate pro-oxidative pathways. AGEs enhance ROS production, further contributing to oxidative stress. Elevated glucose levels also activate the hexosamine pathway, leading to toxic effects and DM complications. In conclusion, OS plays a major role in DM development and complications, though antioxidant interventions have shown limited preventive effects. Understanding oxidative mechanisms in DM can guide future therapeutic strategies.</p>

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The mechanistic interplay of reactive oxygen species in metabolic pathways and insulin signaling in type 2 diabetes

  • 期刊论文

  • 发表日期：

    2025年11月15日

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  • Pandi Selvi Ravi,
  • Shyamaladevi Babu

摘要

Diabetes mellitus is a chronic disorder marked by elevated blood sugar due to insufficient insulin production, reduced insulin sensitivity, or both. The global incidence of diabetes has four-fold the past 20 years, creating a significant health crisis. According to the International Diabetes Federation (2025), around 589 million adults aged 20 to 79 were living with diabetes in 2024. Among this group, more than 9.5 million were affected by type 1 diabetes, including approximately 1.9 million children and adolescents below 20 years of age. By 2050, the global number of individuals with diabetes is anticipated to increase to nearly 853 million. It is classified into type 1 (DM1), which destroys pancreatic β-cells, and type 2 (DM2), primarily linked to insulin resistance. Persistent hyperglycemia in DM causes organ damage, leading to both microvascular and macrovascular complications. OS is crucial in DM’s onset and progression. ROS produced during oxygen metabolism, disrupt cellular metabolic processes and cause oxidative damage. This imbalance between ROS production and antioxidant defences worsens DM complications by impairing insulin production and action. In DM1, ROS reduce β-cell functionality, and hyperglycemia further induces oxidative stress. Key molecular pathways involved in oxidative stress during DM are glycolysis, the hexosamine pathway, PKC activation, and the polyol pathway. Hyperglycemia-induced mitochondrial superoxide inhibits GAPDH, causing glyceraldehyde-3-phosphate to accumulate and activate pro-oxidative pathways. AGEs enhance ROS production, further contributing to oxidative stress. Elevated glucose levels also activate the hexosamine pathway, leading to toxic effects and DM complications. In conclusion, OS plays a major role in DM development and complications, though antioxidant interventions have shown limited preventive effects. Understanding oxidative mechanisms in DM can guide future therapeutic strategies.